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| 1 | Notch信号通路在1-甲基-4-苯基吡啶诱导的人神经母细胞瘤细胞凋亡中的作用显示文摘目的 探讨Notch信号通路在1-甲基-4-苯基吡啶(MPP+)诱导的入神经母细胞瘤细胞凋亡中的活性变化及Notch信号通路抑制剂DAPT对凋亡的调控作用.方法 (1)体外培养的SHSY5Y与不同浓度(0、0.5、1、1.5、2 mmol/L)的MPP+共同孵育0、24、48、72 h.Annexin V-FITC/PI双染及流式细胞术检测细胞凋亡,Western印迹法检测Notch信号通路相关蛋白Notch-1、Jagged-1及Hes-1的表达.(2)将10 μmol/L的γ-分泌酶抑制剂(DAPT)预处理15 min后的SH-SY5Y细胞与1.5 mmol/LMPP+共同孵育48 h,Annexin V-FITC/PI双染及流式细胞术检测细胞凋亡,Western印迹法检测Notch-1、Jagged-1、Hes-1蛋白表达的变化.结果 MPP+以剂量(3.20%±0.19%、10.00%±1.72%、20.60%±3.76%、32.80%±5.12%、46.00%±5.06%,均P< 0.05)和时间(2.80%±0.21%、12.30%±1.82%、19.60%±2.89%、35.00%±4.78%,均P< 0.05)依赖方式诱导SH-SY5Y细胞凋亡,并显著上调Notch信号通路相关蛋白Notch-1、Jagged-1、Hes-1的表达.DAPT可显著抑制MPP+诱导的SH-SY5Y细胞凋亡(3.10% ±0.21%比35.50%±4.98%、19.20%±2.98%,均P< 0.05)以及Notch-1、Jagged-1、Hes-1蛋白的表达.结论 MPP+诱导SH-SY5Y细胞凋亡中Notch信号通路活化,DAPT可阻断Notch信号通路激活,减少MPP+诱导的SH-SY5Y细胞凋亡. | 巴黎 丁雪冰 王雪晶 马明明 何攀 张杰文 | 2014 | 中华医学杂志2014，94，13： | 4 |
| 2 | 端粒酶卡侯体蛋白1干扰慢病毒对口腔鳞状细胞癌细胞裸鼠致瘤作用的研究显示文摘目的 探测端粒酶卡侯体蛋白1(TCAB1)基因沉默对裸鼠移植瘤生长及肿瘤细胞生物学行为的影响。方法 采用定量荧光原位杂交(Q-FISH)方法测定RNA干扰慢病毒sh TCAB1和sh阴性对照(NC)处理后经稳定筛选26代人口腔鳞状细胞癌(OSCC)的Cal27细胞系染色体末端端粒的信号强度。然后将RNA干扰的Cal27细胞接种于裸鼠颈部皮下左、右两侧,定期监测肿瘤体积,绘制肿瘤生长曲线,称取瘤体重量。采用免疫组织化学检测移植瘤组织中TCAB1、B细胞淋巴瘤蛋白-2(Bcl-2)、半胱氨酸天冬氨酸特异性蛋白酶-3、血管内皮生长因子(VEGF)和细胞周期蛋白D1的表达。结果 Q-FISH结果显示,sh TCAB1处理后的Cal27细胞较sh NC处理后及野生型Cal27细胞的端粒平均长度明显缩短。sh TCAB1处理组OSCC移植瘤生长速度明显较sh NC对照组减慢。移植瘤平均重量为0.06 g,对照组为0.26 g,抑瘤率达76.9%。免疫组织化学结果显示,sh TCAB1组移植瘤中TCAB1表达明显降低,同时,Bcl-2、VEGF和细胞周期蛋白D1的表达降低,半胱氨酸天冬氨酸蛋白酶-3的表达升高。结论 sh TCAB1慢病毒能够明显抑制裸鼠人OSCC移植瘤的生长,其抗肿瘤机制与诱导肿瘤细胞凋亡、延长肿瘤细胞分裂周期及抑制血管生成有关。 | 王琨 葛奕辰 崔博淼 苟雅萍 孙崇奎 龙敏 肖丽英 李燕 | 2017 | 国际口腔医学杂志2017，44，1： | 2 |
| 3 | DAPT suppresses the proliferation of human glioma cell line SHG-44显示文摘Objective:To explore the suppressing effect ofγ-secretase inhibitor DAPT on proliferation of human glioma cell line SHG-44 in vitro and its mechanism.Methods:The SHG-44 cell was treated by DAPT with different concentration.The proliferation of cells was detected by MTT assay;cell cycle and TSC of CD133^+were determined by flow cytometry analysis technique;the key factor in Notch signaling pathway(Notch-1,Delta-1,Hes-1)was measured by reverse transcrip tase-polymerase chain reaction and western blotting.Results:DAPT inhibited the growth and proliferation of SHG-44 cells significantly(P<0.05).And the inhibiting effect on SHG-44 cells produced by DAPT showed a dose-dependent manner.DAPT increased the rate of cells in G_0/G_1 phase of SHG-44 cells,while it decreased the rate of cells in S phase.TSC of CD133^+was significantly reduced after DAPT treated SHC-44 cells.The expression of protein and mRNA of Notch-1,Delta-1 and Hes-1 were gradually downregulated with the increase of DAPT doses.Conclusions:DAPT can downregulate these key factor in Notch signaling pathway,reduce the TSC of CD133+and inhibit the proliferation of SHC-44 cells. | Xin Liu Qiu-Ran Xu Wan-Fu Xie Mao-De Wang | 2014 | Asian Pacific Journal of Tropical Medicine2014，7，7： | 1 |
| 4 | Notch信号与细胞凋亡及其在口腔医学的研究进展显示文摘Notch信号通路参与机体多种细胞的凋亡调控,有证据表明在牙齿发育、牙齿损伤与修复、以及口腔肿瘤中均有Notch信号参与并可能与细胞凋亡调控相关。本文就Notch信号对细胞凋亡调控及其在口腔医学领域的研究进展作一综述。 | 尹秋蓉 童娟 王胜朝 | 2015 | 牙体牙髓牙周病学杂志2015，25，2： | 1 |
| 5 | Notch信号通路对细胞凋亡的影响显示文摘Notch信号通路是决定细胞命运的信号通路之一,细胞凋亡和Notch信号通路有着密切的关系,本文将对Notch信号通路对不同类型细胞的凋亡影响及其机制作一综述。 | 黄宽 陈丽 叶军明 蒋琼 | 2016 | 赣南医学院学报2016，36，6： | 1 |
| 6 | DAPT对人胶质瘤细胞系SHG-44增殖的抑制作用及机制显示文摘目的探讨γ-分泌酶抑制剂(DAPT)对人脑胶质瘤细胞系SHG-44细胞体外增殖的抑制作用及机制。方法应用不同浓度的DAPT作用SHG-44细胞,采用MTT法检测细胞增殖情况;流式细胞术检测细胞周期及CD133+的肿瘤干细胞(TSC)数量的变化;应用RT-PCR及Western印迹法检测Notch通路关键分子(Notch-1,Delta-l,Hes-1)基因及蛋白水平的表达。结果 DAPT作用SHG-44细胞后,明显抑制了细胞增殖(P<0.05),且抑制作用呈剂量依赖性。细胞周期结果显示S期细胞比例减少,G0/G1期细胞比例显著增加;CD133+的TSC数量明显减少。随着DAPT浓度的增加,Notch-1,Delta-l,Hes-1 mRNA及蛋白表达水平逐渐下降。结论 DAPT可以下调Notch通路中Notch-l、Delta-1、Hes-1的表达,减少TSC数量,抑制SHG-44细胞增殖。 | 倪伟民 房艳 衣服新 邱建武 丛明 王冰 | 2013 | 中国老年学杂志2013，33，15： | 0 |
| 7 | Regulation of osteoprotegerin expression by Notch signaling in human oral squamous cell carcinoma cell line显示文摘Objective: To investigate the influence of Notch signaling on osteoprotegerin(OPG)expression in a human oral squamous cell carcinoma cell line.Methods: Activation of Notch signaling was performed by seeding cells on Jagged1 immobilized surfaces. In other experiments, a g-secretase inhibitor was added to the culture medium to inhibit intracellular Notch signaling. OPG m RNA and protein were determined by real-time PCR and ELISA, respectively. Finally, publicly available microarray database analysis was performed using connection up- or down-regulation expression analysis of microarrays software.Results: Jagged1-treatment of HSC-4 cells enhanced HES1 and HEY1 m RNA expression, confirming the intracellular activation of Notch signaling. OPG m RNA and protein levels were significantly suppressed upon Jagged1 treatment. Correspondingly, HSC-4 cells treated with a g-secretase inhibitor resulted in a significant reduction of HES1 and HEY1 m RNA levels, and a marked increase in OPG protein expression was observed.These results implied that Notch signaling regulated OPG expression in HSC-4 cells.However, Jagged1 did not alter OPG expression in another human oral squamous cell carcinoma cell line(HSC-5) or a human head and neck squamous cell carcinoma cell line(HN22).Conclusions: Notch signaling regulated OPG expression in an HSC-4 cell line and this mechanism could be cell line specific. | Jeeranan Manokawinchoke Thanaphum Osathanon Prasit Pavasant | 2016 | Asian Pacific Journal of Tropical Biomedicine2016，6，8： | 0 |
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